Role of abciximab in the treatment of coronary artery disease

Glycoprotein IIb/IIIa complex is a crucial membrane receptor for platelet aggregation, binding platelets to fibrinogen and establishing interplatelet bridges. This receptor is the common end point of the multiple activation pathways of a platelet. Antiplatelet agents, such as aspirin or thienopyridines, including ticlopidine and clopidogrel, inhibit one or more but not all, of these pathways. Inhibitors of the receptor are powerful platelet antiaggregants and include two groups of agents: non-competitive receptor blockers, such as abciximab, and competitive antagonists, such as tirofiban and eptifibatide. Abciximab is a monoclonal antibody that binds to the glycoprotein IIb/IIIa complex, thus blocking the interaction with fibrinogen. It is used for treatment of coronary artery disease, being well-studied in the setting of acute coronary syndromes and percutaneous coronary intervention, in which a rapid and effective antiaggregation is clinically important.     

Role of abciximab in the treatment of coronary artery disease

Glycoprotein IIb/IIIa complex is a crucial membrane receptor for platelet aggregation, binding platelets to fibrinogen and establishing interplatelet bridges. This receptor is the common end point of the multiple activation pathways of a platelet. Antiplatelet agents, such as aspirin or thienopyridines, including ticlopidine and clopidogrel, inhibit one or more but not all, of these pathways. Inhibitors of the receptor are powerful platelet antiaggregants and include two groups of agents: non-competitive receptor blockers, such as abciximab, and competitive antagonists, such as tirofiban and eptifibatide. Abciximab is a monoclonal antibody that binds to the glycoprotein IIb/IIIa complex, thus blocking the interaction with fibrinogen. It is used for treatment of coronary artery disease, being well-studied in the setting of acute coronary syndromes and percutaneous coronary intervention, in which a rapid and effective antiaggregation is clinically important.     

Platelet glycoprotein IIb/IIIa-receptor inhibitors in patients with acute coronary syndromes or undergoing percutaneous coronary interventions: a review

BACKGROUND: Over 12.2 million Americans are affected by acute coronary syndromes (ACS) resulting from arterial thrombosis after atherosclerotic plaque rupture. The mechanism of thrombosis is based on the platelet activation pathway, facilitated by expression of the platelet glycoprotein (GP) lIb/Illa receptors. The platelet GP IIb/IIIa-receptor inhibitors represent a new class of drugs, of which abciximab, eptifibatide, and tirofiban have been approved for use in the medical management of ACS and as adjunctive therapy in percutaneous coronary interventions (PCIs). OBJECTIVE: This article reviews the results of published multicenter, randomized, placebo-controlled, double-blind trials of the efficacy and safety of platelet GP IIb/IIIa-receptor inhibitors in patients with coronary artery disease. METHODS: To identify articles for this review, a search of MEDLINE for the years 1994 through 2000 was conducted using the key words myocardial ischemia, unstable angina, angioplasty, stent, abciximab, eptifibatide, tirofiban, lamifiban, and platelet aggregation inhibitors. Relevant review articles were consulted as well as reports of clinical studies. CONCLUSIONS: Three GP IIb/IIIa-receptor inhibitors--abciximab, eptifibatide, and tirofiban-are approved by the US Food and Drug Administration as adjunctive therapy in patients undergoing PCI. Eptifibatide and tirofiban 'are also indicated for the medical management of patients with unstable angina and non-ST-segment-elevation myocardial infarction. The use of GP IIb/IIIa-receptor inhibitors as a component of management with fibrinolytic agents is under investigation. Studies comparing the efficacy of tirofiban and abciximab in patients undergoing planned PCI with intracoronary stent placement are in progress. Until data are available from long-term trials and head-to-head comparisons of these agents, it is not possible to generalize about their overall or comparative efficacy.     

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The glycoprotein (GP) IIb/IIIa receptor serves as the final common pathway of platelet-thrombus formation. Thus, the GP IIb/IIIa receptor has been identified as a target for the prevention of thrombus formation during acute coronary syndromes and/or percutaneous coronary intervention. While there are several intravenous GP IIb/IIIa inhibitors available, abciximab has proven to be a dependable agent with unique properties. Based on American College of Cardiology, American Heart Association and Society for Angiography and Interventions guidelines, compared with the other available intravenous GP IIb/IIIa inhibitors, abciximab receives the highest recommendation for use in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Abciximab is also unique in that there is no need for renal dosing and its effects are mostly reversible with platelet transfusions.     

Abciximab: a review and update for clinicians

The glycoprotein (GP) IIb/IIIa receptor serves as the final common pathway of platelet-thrombus formation. Thus, the GP IIb/IIIa receptor has been identified as a target for the prevention of thrombus formation during acute coronary syndromes and/or percutaneous coronary intervention. While there are several intravenous GP IIb/IIIa inhibitors available, abciximab has proven to be a dependable agent with unique properties. Based on American College of Cardiology, American Heart Association and Society for Angiography and Interventions guidelines, compared with the other available intravenous GP IIb/IIIa inhibitors, abciximab receives the highest recommendation for use in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Abciximab is also unique in that there is no need for renal dosing and its effects are mostly reversible with platelet transfusions.     

The role of tirofiban in acute coronary syndromes

Platelet activation and aggregation play an important and essential role in the formation of intracoronary thrombus in acute coronary syndromes (ACS). ACS still carries unacceptably high rates of morbidity and mortality despite intensive antianginal therapy and the wide use of aspirin and heparin. Two glycoprotein IIb/IIIa receptor inhibitors are now licensed for concomitant use with heparin and aspirin in ACS. Glycoprotein IIb/IIIa receptor inhibitors block the final step for platelet aggregation and fibrinogen binding, thus preventing thrombus formation. Tirofiban is a potent, synthetic, non-peptide and specific glycoprotein IIb/IIIa receptor inhibitor. In three major international trials involving over 7200 patients (PRISM, PRISM-PLUS and RESTORE), tirofiban was shown to be well tolerated and to reduce the risk of ischaemic complications in patients with unstable angina, non-Q-wave myocardial infarction and high-risk patients undergoing revascularisation when used in combination with aspirin and heparin. These and ongoing studies are discussed.     

GLYCOPROTEIN IIB/IIIA ANTAGONISTS: DO THEY HAVE A ROLE IN THE MANAGEMENT OF UNSTABLE ANGINA?

Plaque rupture, platelet aggregation and thrombosis have central roles in the pathogenesis of acute coronary syndromes. Despite several trials showing the benefit of aspirin and heparin in patients presenting with unstable angina and acute myocardial infarction, these patients are still at risk. This has prompted the development and evaluation of several new therapeutic agents including low molecular weight heparin, new antiplatelet drugs (e.g. ticlopidine and clopidogrel), direct thrombin inhibitors, and intravenous and oral glycoprotein IIb/IIIa antagonists. The IIb/IIIa receptor is the final common pathway involved in platelet aggregation. Thus, whatever the stimulus for platelet activation, subsequent aggregation is mediated by the IIb/IIIa receptor binding fibrinogen. A variety of antibody, peptide and non-peptide compounds that block the IIb/IIIa receptor have been developed, and several studies have investigated the role of these agents in patients with acute coronary syndromes both within and outside the setting of percutaneous intervention. This article summarises the studies to date using IIb/IIIa antagonists, and discusses their role in patients with non-ST segment elevation acute coronary syndromes.     

Antiplatelet medications and their indications in preventing and treating coronary thrombosis

Platelets play a pivotal role in the pathophysiology of unstable angina, acute myocardial infarction, and complications following percutaneous coronary intervention. Three classes of platelet-inhibiting drugs, aspirin, thienopyridines and platelet glycoprotein IIb/ IIIa inhibitors, are now commonly used for the prevention and treatment of disorders of coronary artery thrombosis. For the last several decades aspirin has been the sole option for antiplatelet therapy in the treatment and prevention of the manifestations of cardiovascular disease. However, a wider selection of antiplatelet agents, including the thienopyridines (ticlopidine and clopidogrel) and the platelet glycoprotein (GP)IIb/IIIa receptor antagonists, are now available and provide clinicians with the opportunity to potentially improve upon the previous gold standard of aspirin. This review summarizes these drugs and the scientific data that have led to their use in primary and secondary prevention, unstable angina, myocardial infarction, and percutaneous coronary intervention.     

New therapy with monoclonal antibodies--abciximab, chimeric anti-GP IIb/IIIa antibody

Platelet aggregation is now believed to be mediated by fibrinogen binding to activated GP IIb/IIIa. Antigen binding site of mouse anti-human GP IIb/IIIa monoclonal antibody 7E3, which can inhibit fibrinogen binding to activated human platelet GP IIb/IIIa, was combined with constant region of human IgG to reduce immunogenicity. Monovalent Fab of this mouse-human chimeric antibody named abciximab effectively reduced the onset of cardiovascular accidents when administered in combination with heparin and aspirin in patients undergoing coronary interventions. Although several anti-GP IIb/IIIa other than monoclonal antibodies were developed, clinical efficiency of abciximab is still superior to other agents while its effects on preventing myocardial infarction in unstable angina patients are uncertain.     

Antiplatelet therapy in acute coronary syndromes: the emergency physician's perspective

The platelet plays a central role in the pathogenesis of coronary thrombosis after atherosclerotic plaque rupture, and its active inhibition forms a cornerstone of the management of acute coronary syndromes (ACS). Early treatment with clopidogrel in addition to aspirin is more effective than aspirin alone in reducing recurrent ischemic events in patients presenting with ACS, and is a useful adjunct to percutaneous coronary intervention, especially with stenting. There is a potential for increased bleeding complications in patients on clopidogrel therapy who subsequently undergo urgent coronary artery bypass graft surgery. Consequently, many emergency physicians withhold clopidogrel treatment until it is clear that urgent coronary artery bypass graft surgery will not be required. The potential untoward effects seem to be minimized by withholding antiplatelet therapy 3-5 days before surgery. Intravenous glycoprotein (GP) IIb/IIIa receptors inhibitors are also particularly useful in patients who undergo percutaneous coronary intervention, and may have some utility in the medical management of patients with high-risk non-ST-segment elevation ACS, starting in the emergency department. For patients presenting to the emergency department with ACS, the benefits and risks of initiating clopidogrel or GP IIb/IIIa inhibitor therapy need to be considered on an individual basis.     

Antiplatelet medications and their indications in preventing and treating coronary thrombosis

Platelets play a pivotal role in the pathophysiology of unstable angina, acute myocardial infarction, and complications following percutaneous coronary intervention. Three classes of platelet-inhibiting drugs, aspirin, thienopyridines and platelet glycoprotein IIb/IIIa inhibitors, are now commonly used for the prevention and treatment of disorders of coronary artery thrombosis. For the last several decades aspirin has been the sole option for antiplatelet therapy in the treatment and prevention of the manifestations of cardiovascular disease. However, a wider selection of antiplatelet agents, including the thienopyridines (ticlopidine and clopidogrel) and the platelet glycoprotein (GP)IIb/IIIa receptor antagonists, are now available and provide clinicians with the opportunity to potentially improve upon the previous gold standard of aspirin. This review summarizes these drugs and the scientific data that have led to their use in primary and secondary prevention, unstable angina, myocardial infarction, and percutaneous coronary intervention.     

The evolving role of platelet glycoprotein IIb/IIIa inhibitors in the management of acute coronary syndromes.

OBJECTIVE: To briefly discuss the pathophysiology of acute coronary syndromes (ACS) and to present the clinical data currently available regarding the use of platelet glycoprotein (GP) IIb/IIIa inhibitors in the management of ACS. DATA SOURCES: Literature on antithrombotic therapy in ACS was identified using a MEDLINE search (January 1988-September 1998), along with the Agency on Health Care Policy and Research guidelines for the management of unstable angina. Abstracts from recent scientific meetings were also reviewed. STUDY SELECTION: Review articles from the cardiology literature (pathophysiology) and randomized, controlled clinical trials of currently approved platelet GP IIb/IIIa inhibitors in ACS were evaluated. Ex vivo platelet aggregation studies and pharmacology literature were also included. Abstract data were included to illustrate specific points when published literature was not available. DATA EXTRACTION: Study data were evaluated based on study design, outcome parameters, and adverse drug reactions. Clinical information from review articles was evaluated based on applicability to the treatment of ACS. DATA SYNTHESIS: Platelet adhesion and aggregation are pivotal events in the pathophysiology of ACS. The GP IIb/IIIa inhibitors represent a new and unique class of drugs that block fibrinogen and von Willebrand factor-mediated platelet aggregation, the common end point of all biologic pathways of platelet aggregation. Three agents are currently approved by the Food and Drug Administration: abciximab, a monoclonal antibody; eptifibatide, a synthetic peptide; and tirofiban, a synthetic nonpeptide. CONCLUSIONS: Clinical trial data demonstrate efficacy of all three GP IIb/IIIa inhibitors in reducing the combined end point of morbidity and mortality in patients undergoing angioplasty. Eptifibatide and tirofiban also reduce the combined end point of morbidity and mortality in patients with unstable angina. These data expand the present role of platelet GP IIb/IIIa inhibitors by providing evidence for their effectiveness in the medical treatment of ACS. However, the specific role that these agents will have in the management of ACS is yet to be fully defined.     

Glycoprotein IIb/IIIa inhibitors increase COAT-platelet production in vitro

Platelets activated simultaneously with thrombin and collagen reveal a subpopulation of cells that express on their surfaces high levels of several alpha-granule proteins, including factor V and fibrinogen; these COAT platelets (collagen and thrombin-activated platelets) represent roughly 30% of the total population. Evidence of enhanced stability of proteins on the COAT-platelet surface was provided by the observation that PAC-1, a mAB recognizing the activated form of glycoprotein (GP) IIb/IIIa, did not inhibit fibrinogen binding to COAT-platelets. We therefore undertook a systematic evaluation of the effects of other GP IIb/IIIa inhibitors on the production of COAT platelets. Not only did GP IIb/IIIa antagonists fail to inhibit the retention of fibrinogen on COAT-platelets, but several actually increased the absolute percentage of COAT platelets produced. The increases over control values in the presence of eptifibatide, tirofiban, and DMP-802 were 1.36-, 1.20-, and 1.05-fold, respectively (P <.01 for each comparison). COAT-platelet production in the presence of abciximab was not significantly affected. However, platelet activation with thrombin plus ALB6, an Fc-receptor agonist, produces a product, referred to as FcRT platelets, that is indistinguishable from COAT platelets; all 4 GP IIb/IIIa antagonists tested potentiated formation of FcRT platelets. These findings indicate that fibrinogen binding to COAT platelets and FcRT platelets is not affected by available GP IIb/IIIa inhibitors. More importantly, our study demonstrates a potentiation of COAT-platelet production by some GP IIb/IIIa antagonists that may be relevant to the observation that long-term administration of orally available GP IIb/IIIa inhibitors not only failed to protect patients but actually increased the frequency of acute coronary events.     

Nonimmunogenicity of eptifibatide, a cyclic heptapeptide inhibitor of platelet glycoprotein IIb-IIIa

Inhibitors of platelet glycoprotein (GP) IIb-IIIa have been demonstrated to be effective in controlling acute cardiac complications in patients presenting with acute ischemic coronary syndromes (AICS). Since patients with atherosclerotic coronary vascular disease may present with AICS on multiple occasions, it is important to have documented evidence that novel antithrombotic agents are nonimmunogenic and thus safe for repeated administration. Eptifibatide (Integrilin) is a cyclic heptapeptide inhibitor that contains a modified lysine-glycine-aspartic acid sequence that recognizes the binding site of platelet GP IIb-IIIa, resulting in potent and selective inhibition of its binding to fibrinogen. An enzyme-linked immunosorbent assay sensitive to all classes of immunoglobulins was developed to test the immunogenicity of eptifibatide in humans. In two clinical studies, Integrilin to Minimize and Prevent Acute Coronary Thrombosis (IMPACT) and IMPACT II, samples were obtained from 414 patients undergoing coronary angioplasty to determine anti-eptifibatide antibodies at baseline and 30 days after treatment. In a separate clinical pharmacology study, 28 healthy volunteers received 2 infusions of eptifibatide 28 days apart and were monitored at baseline (immediately before the first infusion), at 28 days (immediately before the second infusion), and at 42, 56, 84, and 112 days after enrollment to monitor for an anamnestic anti-eptifibatide response. Eptifibatide administration did not result in an antibody response in any of the 3 studies, even after repeated administration. Eptifibatide represents a potent, specific inhibitor of the platelet GP IIb-IIIa complex that has not been observed to be immunogenic in clinical studies and is thus safe for repeated administration. This finding suggests that small, peptide-based therapeutic agents, which are becoming increasingly common, may be used in humans without inciting an immune response.     

Effect of PlA1/A2 glycoprotein IIIa gene polymorphism on the long-term outcome after successful coronary stenting

Background

Platelet adhesion and subsequent thrombus formation on a subendothelial matrix at the site of vascular damage play a crucial role in the arrest of posttraumatic bleeding but also in different pathological thrombotic events, such as acute coronary syndrome and stroke. Recently published studies have clearly demonstrated that platelet integri αIIbβ3 is intimately involved in the occlusive thrombus formation at the site of endothelial damage. Therefore, any genetic variation in the expression of this receptor may lead to an excessive bleeding or excessive thrombus formation. In this study, we evaluated the influence of HPA-1 polymorphism of integrin αIIbβ3 on platelet adhesion onto immobilized fibrinogen using an in vitro system simulating blood flow.

Methods

Platelets in anticoagulated whole blood [49 healthy previously genotyped blood donors) were labelled with fluorescence dye and perfused through a rectangular flow chamber (shear rates of 50 s^-1, 500 s^-1 and 1500 s^-1). A fluorescence laser-scan microscope was used for visualisation and quantification of platelet adhesion at 15 sec, 1 and 5 minutes after start of perfusion.

Results

During perfusion, the platelet adhesion linearly increased with regard to exposition time and shear rate. Perfusion of blood preincubated with Abciximab over fibrinogen-coated cover-slips showed reduced platelet adherence (absolute fluorescence: 168 ± 35 U vs. 53000 ± 19000 at control experiments, p < 0.05), as well as by perfusion over BSA-coated glass coverslips. Platelet with HPA-1a/1a genotype exhibited initial better adhesion but they also exhibited higher detachment under arterial flow conditions compared to the HPA-1b/1b platelets. Analysis of stable adhesion rate indicate that the platelets carrying the HPA-1b/1b genotype have a higher reactivity threshold for initial interaction with fibrinogen but under the higher shear rate (in regard to time of perfusion) also realize more stable bonds with fibrinogen than platelets with the HPA-1a/1a genotype.

Conclusion

Our data support the contention that genetically determined variants of platelet integrins αIIbβ3 could play a role in arterial thrombogenesis and thus confirm the hypothesis derived from epidemiological studies.     

Present and evolving role of eptifibatide in the treatment of acute coronary syndromes

Platelet-dependent thrombosis plays a central role in the pathophysiology of myonecrosis in both percutaneous coronary interventions (PCIs) and acute coronary syndromes (ACS). Extensive data from randomized clinical trials support the use of acute therapies that interfere with platelet aggregation to provide clinical benefit to patients presenting with ACS and undergoing PCI. Glycoprotein (GP) IIb/IIIa receptor antagonists represent a major advance in the therapy of patients undergoing PCI and those with non-ST segment elevation (NSTE) ACS. Eptifibatide, a small molecule GP IIb/IIIa receptor antagonist, is one such agent. A more consistent platelet-inhibitory effect over time and the short half-life of eptifibatide represent potential pharmacologic advantages compared with other drugs within this class. Large, randomized clinical trials have demonstrated the benefits of eptifibatide for treating patients with NSTE ACS and patients undergoing PCI, establishing its central role in modern management of these conditions. However, recent new advances in the pharmacotherapy of ACS and PCI are requiring us to reconsider the role of GP IIb/IIIa inhibitors; therefore, ongoing and future randomized clinical trials will re-examine GP IIb/IIIa inhibition and establish the role of GP IIb/IIIa inhibitors for the next decade.     

The platelet in diabetes: focus on prevention of ischemic events

Accelerated atherosclerosis and the increased risk of thrombotic vascular events in diabetes may result from dyslipidemia, endothelial dysfunction, platelet hyperreactivity, an impaired fibrinolytic balance, and abnormal blood flow. There is also a correlation between hyperglycemia and cardiovascular (CV) events. The importance of platelets in the atherothrombotic process has led to investigation of using antiplatelet agents to reduce CV risk. A meta-analysis conducted by the Antiplatelet Trialists' Collaboration demonstrated that aspirin reduced the risk of ischemic vascular events as a secondary prevention strategy in numerous high-risk groups, including patients with diabetes. Based on results from placebo-controlled randomized trials, the American Diabetes Association recommends low-dose enteric-coated aspirin as a primary prevention strategy for people with diabetes at high risk for CV events. Clopidogrel is recommended if aspirin allergy is present. There is occasionally a need for an alternative to aspirin or for additive antiplatelet therapy. Aspirin in low doses inhibits thromboxane production by platelets but has little to no effect on other sites of platelet reactivity. Agents such as ticlopidine and clopidogrel inhibit ADP-induced platelet activation, whereas the platelet glycoprotein (Gp) IIb/IIIa complex receptor antagonists block activity at the fibrinogen binding site on the platelet. These agents appear to be useful in acute coronary syndromes (ACSs) in diabetic and nondiabetic patients. A combination of clopidogrel plus aspirin was more effective than placebo plus standard therapy (including aspirin) in reducing a composite CV outcome in patients with unstable angina and non-ST segment elevation myocardial infarction. In a meta-analysis of six trials in diabetic patients with ACSs, intravenous GpIIb-IIIa inhibitors reduced 30-day mortality when compared with control subjects. Results from controlled prospective clinical trials justify the use of enteric-coated low-dose aspirin (81-325 mg) as a primary or secondary prevention strategy in adult diabetic individuals (aged >30 years) at high risk for CV events. Recent studies support the use of clopidogrel in addition to standard therapy, as well as the use of GpIIb-IIIa inhibitors in ACS patients.     

Variability of platelet aggregate dispersal with glycoprotein IIb–IIIa antagonists eptifibatide and abciximab

Summary.  Background:  Utilization of glycoprotein IIb–IIIa (GPIIb–IIIa) inhibitors improves outcomes of patients with acute coronary syndromes (ACS), including those undergoing percutaneous coronary intervention (PCI). These results may be related to the ability of the inhibitors to destabilize coronary thrombi, reduce microembolization, and restore vessel patency. Objective:  To evaluate in vitro the ability of GPIIb–IIIa antagonists, abciximab and eptifibatide, to promote the disaggregation of platelet-rich thrombus. Methods: Antagonist-induced disaggregation was assayed in plasma by aggregometry, as well as in whole blood by point of care and capillary perfusion systems. Fibrinogen dissociation from the platelet surface was quantified by flow cytometry. Results:  Significant disaggregation of 5 μ m ADP-induced aggregates was observed after addition of either agent. The maximum extent and rate of disaggregation were significantly higher with eptifibatide than with abciximab. Both antagonists also dispersed 2 μg mL⁻¹ collagen-induced aggregates, again with eptifibatide having a greater effect. Eptifibatide, but not abciximab (up to 10 μg mL⁻¹), was efficient at dissociating aggregates to single platelets in whole blood and dispersing aggregates that had been aged for 30 min before treatment. Eptifibatide also reduced existing thrombus burden in the perfusion model under arterial flow conditions. A key mechanism of aggregate dispersal was antagonist-induced displacement of platelet-bound fibrinogen, which was greater with eptifibatide, a competitive inhibitor of fibrinogen binding, than with the noncompetitive inhibitor, abciximab. Conclusions:  These results suggest that drug concentration and residence time, along with thrombus extent and age, may be critical determinants in promoting timely recanalization.     

血小板糖蛋白Ⅱb/Ⅲa受体拮抗剂治疗急性冠脉综合征的研究进展

血小板糖蛋白Ⅱb/Ⅲa受体拮抗剂可阻断纤维蛋白原与血小板糖蛋白Ⅱb/Ⅲa受体的结合,有效地抑制血小板的聚集,在急性冠脉综合征治疗中有重要作用。现就国内外有关研究报道作一综述。     

Dissolution of thrombus formed during direct coronary angioplasty with a single 10 mg intracoronary bolus dose of abciximab

Direct coronary angioplasty with stent implantation is an effective treatment for acute myocardial infarction. The use of adjunctive abciximab, a platelet glycoprotein IIb/IIIa receptor antagonist is expensive. We report on three cases of direct coronary angioplasty complicated by extensive thrombus formation that were successfully treated with attenuated dosing of abciximab via the intracoronary route. All patients presented with acute myocardial infarction complicated by cardiogenic shock or eminent cardiogenic shock. Abciximab was administered after balloon dilatation when extensive thrombus formation was noted and persisted despite repeated inflations. In all three patients a single 10 mg vial of intracoronary abciximab was administered, resulting in complete dissolution of thrombus, allowing successful deployment of stents. Thus, a single 10 mg intracoronary bolus dose of abciximab may be sufficient to achieve high local concentrations of antiplatelet activity. This facilitates thrombus dissolution and allows the safe deployment of a stent to normalise intracoronary rheology.